Sodium Excretion Is Controlled by Altering Glomerular Filtration or Tubular Sodium Reabsorption Rates

The two variables that influence sodium and water excretion are the rates of filtration and the rates of reabsorption:

Excretion = Glomerular filtration - Tubular reabsorption

GFR normally is about 180 L/day, tubular reabsorption is 178.5 L/day, and urine excretion is 1.5 L/day. Thus, small changes in GFR or tubular reabsorption potentially can cause large changes in renal excretion. For example, a 5 per cent increase in GFR (to 189 L/day) would cause a 9 L/day increase in urine volume, if tubular compensations did not occur; this would quickly cause catastrophic changes in body fluid volumes. Similarly, small changes in tubular reabsorption, in the absence of compensatory adjustments of GFR, would also lead to dramatic changes in urine volume and sodium excretion. Tubular reabsorption and GFR usually are regulated precisely, so that excretion by the kidneys can be exactly matched to intake of water and electrolytes.

Even with disturbances that alter GFR or tubular reabsorption, changes in urinary excretion are minimized by various buffering mechanisms. For example, if the kidneys become greatly vasodilated and GFR increases (as can occur with certain drugs or high fever), this raises sodium chloride delivery to the tubules, which in turn leads to at least two intrarenal compensations: (1) increased tubular reabsorption of much of the extra sodium chloride filtered, called glomerulotubular balance, and (2) macula densa feedback, in which increased sodium chloride delivery to the distal tubule causes afferent arteriolar constriction and return of GFR toward normal. Likewise, abnormalities of tubular reabsorption in the proximal tubule or loop of Henle are partially compensated for by these same intrarenal feedbacks.

Because neither of these two mechanisms operates perfectly to restore distal sodium chloride delivery all the way back to normal, changes in either GFR or tubular reabsorption can lead to significant changes in urine sodium and water excretion. When this happens, other feedback mechanisms come into play, such as changes in blood pressure and changes in various hormones, that eventually return sodium excretion to equal sodium intake. In the next few sections, we review how these mechanisms operate together to control sodium and water balance and in so doing act also to control extracellular fluid volume. We should keep in mind, however, that all these feedback mechanisms control renal excretion of sodium and water by altering either GFR or tubular reabsorption.

Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance

One of the most basic and powerful mechanisms for control of blood volume and extracellular fluid volume, as well as for the maintenance of sodium and fluid balance, is the effect of blood pressure on sodium and water excretion—called the pressure natriuresis and pressure diuresis mechanisms, respectively. As discussed in Chapter 19, this feedback between the kidneys and the circulatory system also plays a dominant role in long-term blood pressure regulation.

Pressure diuresis refers to the effect of increased blood pressure to raise urinary volume excretion, whereas pressure natriuresis refers to the rise in sodium excretion that occurs with elevated blood pressure. Because pressure diuresis and natriuresis usually occur in parallel, we refer to these mechanisms simply as "pressure natriuresis" in the following discussion.

Figure 29-11 shows the effect of arterial pressure on urinary sodium output. Note that acute increases in blood pressure of 30 to 50 mm Hg cause a twofold to threefold increase in urinary sodium output. This effect is independent of changes in activity of the sympathetic nervous system or of various hormones, such as angiotensin II, Adh, or aldosterone, because pressure natriuresis can be demonstrated in an isolated kidney that has been removed from the influence of these factors. With chronic increases in blood pressure, the effectiveness of pressure natriuresis is greatly enhanced because the increased blood pressure also, after a short time delay, suppresses renin release and, therefore, decreases formation of angiotensin II and aldosterone. As discussed previously, decreased levels of angiotensin II and aldosterone inhibit renal tubular reabsorption of sodium, thereby amplifying the direct effects of increased blood pressure to raise sodium and water excretion.

Pressure Natriuresis and Diuresis Are Key Components of a Renal-Body Fluid Feedback for Regulating Body Fluid Volumes and Arterial Pressure

The effect of increased blood pressure to raise urine output is part of a powerful feedback system that oper-

Arterial pressure (mm Hg)

Figure 29-11

Arterial pressure (mm Hg)

Figure 29-11

Acute and chronic effects of arterial pressure on sodium output by the kidneys (pressure natriuresis). Note that chronic increases in arterial pressure cause much greater increases in sodium output than those measured during acute increases in arterial pressure.

ates to maintain balance between fluid intake and output, as shown in Figure 29-12. This is the same mechanism that is discussed in Chapter 19 for arterial pressure control. The extracellular fluid volume, blood volume, cardiac output, arterial pressure, and urine output are all controlled at the same time as separate parts of this basic feedback mechanism.

During changes in sodium and fluid intake, this feedback mechanism helps to maintain fluid balance and to minimize changes in blood volume, extracellular fluid volume, and arterial pressure as follows:

1. An increase in fluid intake (assuming that sodium accompanies the fluid intake) above the level of urine output causes a temporary accumulation of fluid in the body.

2. As long as fluid intake exceeds urine output, fluid accumulates in the blood and interstitial spaces, causing parallel increases in blood volume and extracellular fluid volume. As discussed later, the actual increases in these variables are usually small because of the effectiveness of this feedback.

3. An increase in blood volume raises mean circulatory filling pressure.

4. An increase in mean circulatory filling pressure raises the pressure gradient for venous return.

5. An increased pressure gradient for venous return elevates cardiac output.

6. An increased cardiac output raises arterial pressure.

7. An increased arterial pressure increases urine output by way of pressure diuresis. The steepness of the normal pressure natriuresis relation indicates that only a slight increase in blood pressure is required to raise urinary excretion severalfold.

8. The increased fluid excretion balances the increased intake, and further accumulation of fluid is prevented.

Basic renal-body fluid feedback mechanism for control of blood volume, extracellular fluid volume, and arterial pressure. Solid lines indicate positive effects, and dashed lines indicate negative effects.

Nephrology Intake Sheet

Figure 29-12

Basic renal-body fluid feedback mechanism for control of blood volume, extracellular fluid volume, and arterial pressure. Solid lines indicate positive effects, and dashed lines indicate negative effects.

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  • Juan
    Which hormones alter reabsorption rate of sodium chloride in the urine?
    8 months ago

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